Vasopressin administration facilitates fluid removal during hemodialysis

Abstract

Inadequate secretion of vasopressin during fluid removal by hemodialysis may contribute to the cardiovascular instability that complicates this therapy and administration of exogenous hormone, by supporting arterial pressure, may facilitate volume removal. To test this, we measured plasma vasopressin in patients with end-stage renal disease (ESRD) during hemodialysis and found that despite significant fluid removal, plasma vasopressin concentration did not increase. We further found that ESRD did not alter the endogenous removal rate of plasma vasopressin and that plasma hormone is not dialyzed. Finally, in a randomized, double-blinded, placebo-controlled trial in 22 hypertensive patients, we examined the effect of a constant infusion of a non-pressor dose of vasopressin on the arterial pressure response during a hemodialysis in which the target fluid loss was increased by 0.5 kg over the baseline prescription. We found that arterial pressure was more stable in the patients receiving vasopressin and that while only one patient (9%) in the vasopressin group had a symptomatic hypotensive episode, 64% of the patients receiving placebo had such an episode (P=0.024). Moreover, increased fluid removal was achieved only in the vasopressin group (520+/-90 ml vs 64+/-130 ml, P=0.01). Thus, administration of non-pressor doses of vasopressin to hypertensive subjects improves cardiovascular stability during hemodialysis and allows increased removal of excess extracellular fluid. Inadequate vasopressin secretion during hemodialysis-induced fluid removal is a likely contributor to the intradialytic hypotension that limits fluid removal.

Serum Vasopressin Response in Patients With Intradialytic Hypotension

“…As seen in Table 2, there was no difference in serum sodium concentrations between the two groups. Previous studies demonstrate that neither hemodialysis nor ultrafiltration prevents a proportionate increase in AVP concentrations during AVP infusion (19). This suggests that AVP concentration is not affected by hemodialysis and ultrafiltration, so AVP removal cannot explain the results found in this study.…”

“…Intravenous vasopressin, as recently shown in non-IDH patients (19), and perhaps intranasal vasopressin administration, may improve hemodynamic stability in an otherwise difficult to treat population.…”

“…Also, a true matched control group was not used in the study. More recently, in an important observation by van der Zee et al, subpressor doses of intravenous vasopressin provided hemodynamic benefit and prevented hypotension during dialysis with ultrafiltration in 22 hypertensive hemodialysis patients (19). They also measured serum AVP levels in 10 normotensive patients during hemodialysis, but the significance of these values is difficult to interpret because they were not from IDH patients.…”

“…A study in 23 hemodialysis patients published more than 10 yr ago demonstrated vasopressin insufficiency as a possible mechanism of IDH in ESRD patients (18). A recent study also demonstrated a hemodynamic benefit with subpressor doses of vasopressin in 22 hypertensive patients during hemodialysis with ultrafiltration (19). Both studies shed important insight into the role of vasopressin in hemodynamic stability.…”

Effect of Hemodialysis on the Hemodynamic Status for Patients with Chronic Renal Failure

“…Another studies reported that heart rate control is initiated and coordinated by pacemaker cells; sympathetic stimulation is associated with release of nor adrenaline , which binds to be adrenergic receptors, whereas parasympathetic stimulation is mediated by acetylcholine release, which binds to M2 muscarinergic receptors [14]. In uremia patients, increased plasma and tissue levels of catecholamine and resistance to their physiologic effect were reported by several authors [15,16,17].Clinical and laboratory evidence suggests that both B-adrenoreceptor and muscarinergic receptor -mediated responses are attenuated in the uremia state [18,19].…”